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To investigate the androgen receptor (AR) isoform expressions in human prostatic cancer tissue and LNCaP cell line.With high resolution isoelectric focusing (IEF) method we demonstrated the different expressions of AR isoforms in human prostatic cancer tissues and LNCaP cell line.Data were obtained from three prostatic cancer specimens and the LNCaP cell line. Three types of AR isoforms were detected with pI values at 6.5, 6.0, and 5.3. For the 3 prostatic cancer specimens, 1 sample showed all the three types of AR isoforms, the second specimen expressed at 6.5 and 6.0, and the third failed to show any type of isoforms. The LNCaP cell line expressed all the three AR isoforms. Binding of 3H-dihydrotestosterone (3H-DHT) to these three isoforms was inhibited by the addition of 100-fold excess of DHT or testosterone, while not by progesterone, oestradiol and diethylstilboestrol.The expression of AR isoforms is different in different prostate cancer tissues, which may be related to the difference in the effect of anti-androgen therapy in different patients.

To study the apoptotic rate (AR) and the androgen and estrogen milieu in the proximal and distal ductal systems of prostate, in order to help exploring the effects of these factors on prostatic growth and the pathogenesis of benign prostatic hypertrophy (BPH).The proximal and distal ends of the ductal system were incised from 20 normal prostate as well as the hypertrophic prostate tissue from 20 patients with BPH. The AR was determined by the DNA end-labeling method and dihydrotestosterone (DHT) and estrodiol (E2), by radioimmunoassay.There was no significant difference in DHT and E2 density between the proximal and distal ends of the ductal systems in normal prostate. E2 appeared to be higher in BPH than in normal prostatic tissues, but the difference was statistically insignificant. In normal prostatic tissue, the AR was significantly higher in the distal than in the proximal ends of the ductal system (P0.05), while the AR of the proximal ends was significantly higher (P0.01) than that in the BPH tissue. No significant correlation was noted between the DHT and E2 density and the AR both in the normal prostate and BPH tissues.The paper is the first time describing a difference in AR in different regions of the ductal system of normal prostate, while the hormonal milieu is similar, indicating a functional inhomogeneity of these regions. A low AR in the proximal duct, where BPH originates, and an even lower AR in the BPH tissue, suggesting the participation of apoptosis in the BPH pathogenesis.

To investigate the androgen receptor (AR) isoforms and its variability of expression in human and rat prostatic tissues.Human benign prostatic hyperplasia (BPH) and prostatic cancer tissues were obtained from patients undergoing prostatectomy, and rat ventral prostate was incised 3 days after castration. Forty-one AR-positive BPH specimens, 3 prostatic cancer specimens, and 6 rat prostates were used. After processing at 4 degrees C, the tissues were examined by means of high resolution isoelectric focusing (IEF) technique to determine their AR isoforms.From the prostatic specimens, 3 types of AR isoforms were detected with pI values at 6.5, 6.0, and 5.3. In human BPH tissues, 15/41 (36.6%) specimens showed all the three types of isoforms, while 19/41 (46.3%) showed 2 isoforms at various combinations and 7/41 (17.1%), 1 isoform. For the 3 prostatic cancer specimens, one showed 3 isoforms, one, 2 isoforms, and the other failed to show any isoform. All rat prostatic tissues showed 2 isoforms at different combinations. Binding of 3H-dihydrotestosterone (DHT) to the isoforms was inhibited by the addition of 100-fold excess of DHT or testosterone, but not progesterone, oestradiol or diethylstilboestrol.AR isoforms are different in different patients. Although their genesis is not clear, the therapeutic implication of the present observation appears to be interesting, that may help clarifying the individual differences in the response to hormonal therapy.